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DC Field | Value | Language |
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dc.contributor.author | Haupt Y. | en |
dc.contributor.author | Lowe S.W. | en |
dc.contributor.author | Haupt S. | en |
dc.contributor.author | Opat S. | en |
dc.contributor.author | Shortt J. | en |
dc.contributor.author | Wolyniec K. | en |
dc.contributor.author | De Stanchina E. | en |
dc.contributor.author | Levav-Cohen Y. | en |
dc.contributor.author | Alsheich-Bartok O. | en |
dc.contributor.author | Louria-Hayon I. | en |
dc.contributor.author | Corneille V. | en |
dc.contributor.author | Kumar B. | en |
dc.contributor.author | Woods S.J. | en |
dc.contributor.author | Johnstone R.W. | en |
dc.contributor.author | Scott C.L. | en |
dc.contributor.author | Segal D. | en |
dc.contributor.author | Pandolfi P.P. | en |
dc.contributor.author | Fox S. | en |
dc.contributor.author | Strasser A. | en |
dc.contributor.author | Jiang Y.-H. | en |
dc.date.accessioned | 2021-05-14T09:32:56Z | en |
dc.date.available | 2021-05-14T09:32:56Z | en |
dc.date.copyright | 2012 | en |
dc.date.created | 20120813 | en |
dc.date.issued | 2012-08-13 | en |
dc.identifier.citation | Blood. 120 (4) (pp 822-832), 2012. Date of Publication: 26 Jul 2012. | en |
dc.identifier.issn | 0006-4971 | en |
dc.identifier.uri | https://repository.monashhealth.org/monashhealthjspui/handle/1/28356 | en |
dc.description.abstract | Neoplastic transformation requires the elimination of key tumor suppressors, which may result from E3 ligase-mediated proteasomal degradation. We previously demonstrated a key role for the E3 ubiquitin ligase E6AP in the regulation of promyelocytic leukemia protein (PML) stability and formation of PML nuclear bodies. Here, we report the involvement of the E6AP-PML axis in B-cell lymphoma development. A partial loss of E6AP attenuated Myc-induced B-cell lymphomagenesis. This tumor suppressive action was achieved by the induction of cellular senescence. B-cell lymphomas deficient for E6AP expressed elevated levels of PML and PML-nuclear bodies with a concomitant increase in markers of cellular senescence, including p21, H3K9me3, and p16. Consistently, PML deficiency accelerated the rate of Myc-induced B-cell lymphomagenesis. Importantly, E6AP expression was elevated in ~ 60% of human Burkitt lymphomas, and down-regulation of E6AP in B-lymphoma cells restored PML expression with a concurrent induction of cellular senescence in these cells. Our findings demonstrate that E6AP-mediated down-regulation of PML-induced senescence is essential for B-cell lymphoma progression. This provides a molecular explanation for the down-regulation of PML observed in non-Hodgkin lymphomas, thereby suggesting a novel therapeutic approach for restoration of tumor suppression in B-cell lymphoma. © 2012 by The American Society of Hematology. | en |
dc.language | English | en |
dc.language | en | en |
dc.publisher | American Society of Hematology (1900 M Street, Suite 2000, Washington DC 20036, United States) | en |
dc.title | E6AP ubiquitin ligase regulates PML-induced senescence in Myc-driven lymphomagenesis. | en |
dc.type | Article | en |
dc.identifier.doi | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1182/blood-2011-10-387647 | en |
dc.publisher.place | United States | en |
dc.identifier.pubmedid | 22689861 [http://www.ncbi.nlm.nih.gov/pubmed/?term=22689861] | en |
dc.identifier.source | 365349300 | en |
dc.identifier.institution | (Wolyniec, Shortt, Corneille, Woods, Johnstone, Fox, Haupt, Haupt) Research Division, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia (Wolyniec, Corneille, Woods, Johnstone, Fox, Haupt, Haupt) Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia (Shortt, Opat) Department of Clinical Haematology, Monash Medical Centre, Clayton, VIC, Australia (De Stanchina, Lowe) Memorial Sloan-Kettering Cancer Center, New York, NY, United States (Levav-Cohen, Alsheich-Bartok, Louria-Hayon) Hebrew University Hadassah Medical School, Jerusalem, Israel (Kumar) Department of Anatomical Pathology, Southern Health, VIC, Australia (Scott, Segal, Strasser) Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, Australia (Scott, Strasser) Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia (Pandolfi) Beth Israel Deaconess Cancer Center, Departments of Medicine and Pathology, Harvard Medical School, Boston, MA, United States (Jiang) Division of Medical Genetics, Department of Pediatrics and Neurobiology, Duke University School of Medicine, Durham, NC, United States (Haupt) Department of Pathology, University of Melbourne, Parkville, VIC, Australia (Haupt) Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC, Australia (Louria-Hayon) Samuel Lunenfeld Research Institute, Mt. Sinai Hospital, Toronto, ON, Australia | en |
dc.description.address | Y. Haupt, Research Division, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia. E-mail: ygal.haupt@petermac.org | en |
dc.description.publicationstatus | Embase | en |
dc.rights.statement | Copyright 2012 Elsevier B.V., All rights reserved. | en |
dc.identifier.authoremail | Haupt Y.; ygal.haupt@petermac.org | en |
item.cerifentitytype | Publications | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | none | - |
item.openairetype | Article | - |
crisitem.author.dept | Haematology | - |
crisitem.author.dept | Haematology | - |
crisitem.author.dept | Pathology | - |
Appears in Collections: | Articles |
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